ライフサイエンスコーパス: MCF-7 cell

1 both, or absence of any such protrusions in MCF-7 cells.

2 gligible binding to alpha(v)beta(3)-negative MCF-7 cells.

3 by RNAi further promotes VEGF expression in MCF-7 cells.

4 to characterize estrogen responsive genes in MCF-7 cells.

5 dance change is observed for less-metastasis MCF-7 cells.

6 ably reduced, PRNP and ERLEC1 mRNA levels in MCF-7 cells.

7 dynamics of individual microtubules in live MCF-7 cells.

8 r RBP SRSF5 affects splicing of Mcl-1 in the MCF-7 cells.

9 the genome at near-nucleotide resolution in MCF-7 cells.

10 produced and used for uptake experiments in MCF-7 cells.

11 were detected in tamoxifen-resistant (TAM-R) MCF-7 cells.

12 intracellular secretory vesicles in HC11 and MCF-7 cells.

13 phosphorylation and nuclear accumulation in MCF-7 cells.

14 ac1 abolished tRA-induced phosphorylation in MCF-7 cells.

15 ively), the tRA-stimulated NIS expression in MCF-7 cells.

16 nd p38beta for the full expression of NIS in MCF-7 cells.

17 e-Guerin levels in mammary epithelial cancer MCF-7 cells.

18 ionally interact at target gene promoters in MCF-7 cells.

19 erentially induce apoptosis over necrosis in MCF-7 cells.

20 duce G(0)/G(1) growth arrest of asynchronous MCF-7 cells.

21 dependently induce an MDR1/P-gp phenotype in MCF-7 cells.

22 regulated by 4-OHT via endogenous ERbeta in MCF-7 cells.

23 transcriptional activation and expression in MCF-7 cells.

24 OHT(R) cells and increased in TIMP3-depleted MCF-7 cells.

25 Cs and no or weak cell-cell interactions for MCF-7 cells.

26 in rabbit reticulocyte lysate, bacteria, and MCF-7 cells.

27 vealed promising anticancer activity against MCF-7 cells.

28 K1, but not SphK2, increased S1P export from MCF-7 cells.

29 ptional activity and protein accumulation in MCF-7 cells.

30 in MCF-7-T-bet cells and in insulin-treated MCF-7 cells.

31 YPIB1 were both inducible by dioxin in human MCF-7 cells.

32 n estrogen receptor alpha (ERalpha)-positive MCF-7 cells.

33 ed rapid release of S1P and dihydro-S1P from MCF-7 cells.

34 F promoter in a P-TEFb-independent manner in MCF-7 cells.

35 observation that miR-19 levels are higher in MCF-7 cells.

36 RA also induced rapid activation of Akt in MCF-7 cells.

37 , miR-21, by activating estrogen receptor in MCF-7 cells.

38 gate was passed over a monolayer of cultured MCF-7 cells.

39 HeLa cells, while miR-155 was quantified in MCF-7 cells.

40 lpha binding to estrogen-responsive genes in MCF-7 cells.

41 cells and in low migratory breast carcinoma MCF-7 cells.

42 ced activation of p38 in human breast cancer MCF-7 cells.

43 ntration of 2nM) on electrochemical activity MCF-7 cells.

44 and morphological changes of MDA-MB-231 and MCF-7 cells.

45 tive response in human breast adenocarcinoma MCF-7 cells.

46 activity and thus increased miR-221 level in MCF-7 cells.

47 ntargeted mass-spectroscopy metabolomics for MCF-7 cells.

48 hIP-BIT as being differentially expressed in MCF-7 cells.

49 ha1,2- and alpha1,3 fucose linkages found in MCF-7 cells.

50 currence of open compartments on chr16-22 in MCF-7 cells.

51 equent interactions than are observed in the MCF-7 cells.

52 K signaling to support junctional tension in MCF-7 cells.

53 actor)-mediated activation of ERK and AKT in MCF-7 cells.

54 ading to increased migration and invasion in MCF-7 cells.

55 s candidates for regulation were examined in MCF-7 cells.

56 level is low but inducible by epirubicin in MCF-7 cells.

57 ing sequence and expressed these proteins in MCF-7 cells.

58 late the proliferation of estrogen-sensitive MCF-7 cells.

59 binding of WA to Cys(303) of beta-tubulin in MCF-7 cells.

60 blockade) and depolymerization of tubulin in MCF-7 cells.

61 moter also occurs in human Hep3B, HepG2, and MCF-7 cells.

62 ntracellular ATP and GTP imaging in cultured MCF-7 cells.

63 rnalization at MI=1.0, 79.5% at MI=1.5) than MCF-7 cells (42.4% internalization at MI=1.0, 35.7% at M

64 MCF-7 cells, a human breast adenocarcinoma, were retaine

65 In human Huh7 and MCF-7 cells, a VACV mutant lacking both K1L and C7L (vK1

66 knockdown of p62 by small interfering RNA in MCF-7 cells abrogates Vps34-dependent tumor growth.

67 creased by 1.60 nmol (61.1 %) in 3.0 x 10(6) MCF-7 cells after 100 nM insulin stimulation.

68 -dose coexposures of human mammary carcinoma MCF-7 cells against polycyclic aromatic hydrocarbons (PA

69 -UTR negatively regulates gene expression in MCF-7 cells, an effect reversed by deletion of the miR-1

70 d deprivation is significantly attenuated in MCF-7 cells, an ER-positive breast cancer cell line, whe

71 vels of immunoreactive phosphoAkt in treated MCF-7 cells and bound to immobilized ganglioside GT1b.

72 d the dynamics of individual microtubules in MCF-7 cells and delayed the reassembly of depolymerized

73 Both senescence of MCF-7 cells and differentiation of MDA-MB-231 cells were

74 e cellular uptake of the monodisperse CDs in MCF-7 cells and Huh-7 liver cancer cells.

75 r component of ATRA-induced growth arrest of MCF-7 cells and identify S6K as a novel downstream targe

76 n of Trask expression and phosphorylation in MCF-7 cells and in 3T3v-src cells was associated with a

77 05-ERbeta nuclear speckles were also seen in MCF-7 cells and markedly increased in size and number at

78 tion of receptor PTPepsilon (RPTPepsilon) in MCF-7 cells and MDA-MB-231 upon PMA, FGF, and serum stim

79 formance for the ultrasensitive detection of MCF-7 cells and quantification of cell surface glycan.

80 ate in MCF-7/MX100 cells but not in parental MCF-7 cells and sensitized the MDR cells to the chemothe

81 TPSF reduces ERalpha protein levels in MCF-7 cells and several other cell lines without alterin

82 shed for complex 5.Let against breast cancer MCF-7 cells and significantly lower activity against gli

83 ignificantly elevated in tamoxifen-resistant MCF-7 cells and T47D cells.

84 ression to be basally repressed by Nkx3-1 in MCF-7 cells and TOT treatment appeared to elevate Nkx3-1

85 e deglycoBLM conjugate, bound selectively to MCF-7 cells and were internalized.

86 In MCF-7 cells and xenograft tumors, MnO2 /DVDMS is reduced

87 to adenosine 5'-diphosphate or tumor cells (MCF-7 cells) and exhibited a decreased angiogenic potent

88 ty to penetrate the cell membrane in 3T3 and MCF-7 cells, and cationic PNAs were found to be accumula

89 nhances UVC irradiation-induced apoptosis in MCF-7 cells, and causes sensitization to DNA-damaging dr

90 cell growth: it showed IC(5)(0) = 1.0 nM in MCF-7 cells, and it was uniformly active in the whole pa

91 duces endogenous tissue factor expression in MCF-7 cells, and overexpression of miR-19 down-regulates

92 s was dramatically reduced in the Cav-1 null MCF-7 cells, and PIV-5 grown in MCF-7 cells had a reduce

93 n bone marrow, multiple leukemia cell lines, MCF-7 cells, and subjects after GM-CSF treatment but not

94 rogen responsive element (ERE)-luciferase in MCF-7 cells, and Tff1 mRNA in T47D cells.

95 ycin-derivatized microbubbles adhered to the MCF-7 cells, and the association could be monitored by t

96 RB inactivation increases IL-6 production in MCF-7 cells appeared to involve fatty acid oxidation (FA

97 The effects of BJ3Z cells on MCF-7 cells are equivalent to those of E(2).

98 A and increased with OTUB1 overexpression in MCF-7 cells, arguing that OTUB1 positively regulates FOX

99 Using MCF-7 cells as a model system, we show that ATRA stimula

100 Using MCF-7 cells as in vitro model for anti-cancer mechanisti

101 tro, disrupted the microtubular structure in MCF-7 cells as visualized by confocal microscopy, and ca

102 ds preferentially to tissue factor 3'-UTR in MCF-7 cells, as compared with MDA-MB-231 cells, consiste

103 addressing the effect of 17beta-estradiol on MCF-7 cells at early (3-4 hours) and late (24 hours) tim

104 morphology and subcellular structure within MCF-7 cells at several time points after treatment with

105 Similarly, in MCF-7 cells, BCAR3-induced tyrosine phosphorylation of t

106 growth in vitro and uterine enlargement and MCF-7 cell breast cancer xenograft growth in vivo were s

107 In MCF-7 cells, BS-181 inhibited the phosphorylation of CDK

108 cited cytosolic Ca(2+) increases not only in MCF-7 cells but also in ER-negative SKBr3 cells.

109 nificant decrease in Mcl-1 protein levels in MCF-7 cells but an increase in JAR cells, respectively,

110 regulation of ER transcriptional activity in MCF-7 cells but decreased ER protein levels and transcri

111 ndependent E(2)-ERalpha-stimulated growth of MCF-7 cells but does not inhibit growth of ER-negative M

112 nse element-dependent luciferase activity in MCF-7 cells but not in MCF-7 stable cells expressing app

113 time-dependent manner in the drug-sensitive MCF-7 cells but not in the resistant counterparts in res

114 Inactive pro-invasive genes in MCF-7 cells but not in U251 cells frequently exhibited a

115 riphosphate receptor mediated in ER-positive MCF-7 cells but transitory and ryanodine receptor mediat

116 on reduced upon genotoxic agent treatment in MCF-7 cells, but remained relatively constant in resista

117 on of ERbeta1 promoted growth suppression in MCF-7 cells, but the anti-proliferative effects of ERbet

118 These TPEs all stimulate growth in MCF-7 cells, but unlike the planar estrogens they block

119 Global transcript profiling of MCF-7 cells by RNA-seq shows that FDI-6 specifically dow

120 nstrated that the ectopic EPSTI1 granted the MCF-7 cells capability of both invasive growth in the br

121 These approaches achieved MCF-7 cell capture from </=10 microL of whole blood with

122 Using an MCF-7 cell cDNA library in a yeast two-hybrid screen, we

123 as observed for the viability of HCT 116 and MCF-7 cells challenged with 0.4, 4.0, and 40mug/ml nanoe

124 [Deltaf] and motional resistance DeltaR) of MCF-7 cells compared with those of HMECs mirror the canc

125 MCF-7 cells concentrated in S-phase or G0/G1-phase were

126 de based platform for breast cancer specific MCF-7 cell concentration estimation and their molecular

127 des were exposed to solutions with different MCF-7 cell concentrations and CV technique was used to d

128 and cellular characterization using U937 and MCF-7 cells confirmed that many of these analogues displ

129 A tumor xenograft with Mel-18 knockdown MCF-7 cells consistently showed increased ZEB1 and ZEB2

130 ater) from seven individuals, and (iv) human MCF-7 cells cultured in vitro (Kcell/water).

131 ma hyorhinis-infected human breast carcinoma MCF-7 cell cultures (MCF-7.Hyor), depending on the prope

132 and assays involving microscopy imaging and MCF-7 cells culturing can be performed in 2-3 d.

133 ther, flow cytometry showed that G-1 blocked MCF-7 cell cycle progression at the G(1) phase.

134 Silencing EDI3 in MCF-7 cells decreased this enzymatic activity, increased

135 The IC50 of DHA or EPA in MCF-7 cells decreased when combined with E2 (10 nM) trea

136 Co-immunoprecipitation studies in MCF-7 cells demonstrated a direct interaction between p3

137 injections in mice with human breast cancer MCF-7 cells depleted for SMAR1 showed increased CD44 var

138 Importantly, MCF-7 cell-derived exosomes that are caspase-3-deficient

139 ata and RNA polymerase II ChIA-PET data from MCF-7 cells did not suggest remote effects of the enhanc

140 net-based separation for the isolation of 50 MCF-7 cells directly from whole blood.

141 ion of ERalpha by RNA interference (RNAi) in MCF-7 cells downregulated FOXM1 expression.

142 Emergence of antiestrogen-resistant cells in MCF-7 cells during suppression of estrogen signaling is

143 s well as in its ability to degrade Her-2 in MCF-7 cells (EC(50) = 14 vs 38 nM).

144 Autocrine activation of STAT3 in MCF-7 cells ectopically expressing OSM-induced cellular

145 Transcriptomes of MCF-7 cells exposed to varying concentrations of represe

146 MCF-7 cells express all three RAR isoforms, alpha, beta,

147 RNAs to stably knock down PARP-1 or PARG in MCF-7 cells followed by expression microarray analyses.

148 ell viability and abrogate DSBs sustained by MCF-7 cells following epirubicin, owing to an enhancemen

149 rphyrazines with EC50 values as low as 5 nM (MCF-7 cells) for the best compound; this activity was se

150 in normal and neoplastic endometrium and in MCF-7 cells, forms a stable RNA quadruplex demonstrable

151 was the most potent extract, particularly in MCF-7 cells (GI(50) 25.2+/-0.2 mug/ml).

152 Additionally, in MCF-7 cells, GPR30 depletion blocked E(2)-induced and G-

153 Cytoplasmic extracts of MCF-7 cells grown under hypoxia (1% oxygen) recapitulate

154 Supporting this, G-1 profoundly inhibited MCF-7 cell growth, potentially via p53 and p21 induction

155 was to promote SKBr3 cell growth but reduce MCF-7 cell growth.

156 e Cav-1 null MCF-7 cells, and PIV-5 grown in MCF-7 cells had a reduced infectivity.

157 We have previously demonstrated that MCF-7 cells, human breast cancer cells, exhibit the roll

158 ession of tissue factor cDNA was achieved in MCF-7 cells, implying that the 3'-UTR of the tissue fact

159 toxicity and enhance accumulation of ZnPc in MCF-7 cells, improving apoptotic cell death upon irradia

160 lso inhibited self-assembly of KGN, NHF, and MCF-7 cells in a dose-dependent manner that was specific

161 s on the proliferation of estrogen-dependent MCF-7 cells in a dose-dependent manner, primarily as a l

162 on of JARID1B resulted in an accumulation of MCF-7 cells in G(1).

163 S105-ERbeta levels increased in MCF-7 cells in response to 17beta-estradiol, the ERbeta-

164 ft agar and suppresses the tumorigenicity of MCF-7 cells in severe combined immunodeficiency mice.

165 pCAM/LC-SPDP/Au based biosensor could detect MCF-7 cells in the range of 1x10(5)-1x10(8) with correla

166 loyed a genetically engineered line of human MCF-7 cells in which the levels of transgenic HMGA1 prot

167 To investigate this, we used MCF-7 cells, in which EGF-induced transient ERK activati

168 ere screened for cytoprotective potential in MCF-7 cells, including the mitochondrial membrane potent

169 Overexpression of nuclear-targeted AKT1 in MCF-7 cells increased cell proliferation without comprom

170 The motility of MCF-7 cells increases following expression of a human PM

171 by blockade of beta-adrenergic signaling in MCF-7 cells, indicating that catecholamines were the res

172 quantification of pY in human breast cancer MCF-7 cells, indicating that pY increased by 1.60 nmol (

173 sphorylation of HER1, HER2, HER3 and HER4 in MCF-7 cells, indicative of activation of these proteins.

174 ic expression of functionally active PAR1 in MCF-7 cells induced a hormone-refractory, invasive pheno

175 , expression of BCL-2 blocks death of C6 and MCF-7 cells induced by dominant-negative ATF5, and deple

176 Furthermore, MCF-7 cells intermixed with 1 mL blood and loaded onto l

177 17beta-Estradiol stimulation of MCF-7 cells is a widely used model in the growth of brea

178 indings indicate that RA induction of NIS in MCF-7 cells is mediated by rapid activation of the PI3K

179 pic expression of EPSTI1 in the non-invasive MCF-7 cells is sufficient to induce the cell invasion.

180 Estrogen receptor-positive MCF-7 cells lack caspase-3 and were not responsive to GA

181 Human MCF-7 cells lacking functional FADS2-mediated Delta6-des

182 It subsequently interacted with the MCF-7 cell layer, distributed in the lung, heart and fat

183 CTP by short hairpin RNA in breast carcinoma MCF-7 cells leads to the declined repair efficiency for

184 ive activation of CXCR4 in poorly metastatic MCF-7 cells led to enhanced tumor growth and metastases

185 gene expression profiling strategy with the MCF-7 cell line as a model.

186 8 out of 10 fusion events identified in the MCF-7 cell line in an earlier study.

187 aving PTEN promoter methylated (as in, e.g., MCF-7 cell line).

188 n neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depe

189 ide population (NSP or main population) from MCF-7 cell line, and evaluated the impact of CCN5 on the

190 rmacologic properties were documented in the MCF-7 cell line, and prolactin synthesis was assessed in

191 in decreased expression of miRNA-200b in the MCF-7 cell line.

192 atively low utilization in the less invasive MCF-7 cell line.

193 a metastatic phenotype on the nonmetastatic MCF-7 cell line.

194 changes of these two TSGs in a breast cancer MCF-7 cell line.

195 nstrated profound cytotoxic activity against MCF-7 cell line.

196 A case study on data from MCF-7 cell-line reveals that PEDAL can identify successf

197 micromolar level against the HT-29, M21, and MCF-7 cell lines and blocked cell cycle progression in S

198 Conversely, stable MCF-7 cell lines expressing inducible high levels of ect

199 ork reports the impedance characteristics of MCF-7 cell lines treated with anticancer drug ZD6474 to

200 in solitary cells of GM14667, MDA-MB-231 and MCF-7 cell lines, achieving a DNA amplification efficien

201 ited the strongest cytotoxicity against both MCF-7 cell lines, over 2-fold greater than CA and Lgr, a

202 ive phenotype on minimally invasive HeLa and MCF-7 cell lines.

203 ere achieved for the detection of ERalpha in MCF-7 cell lysate.

204 Notably, in MCF-7 cell mammospheres, which display a well-defined ac

205 expression of CREB3L1 in human breast cancer MCF-7 cells markedly enhanced the sensitivity of these c

206 had previously shown that p23-overexpressing MCF-7 cells (MCF-7+p23) exhibit increased invasion witho

207 pitulated through overexpression of T-bet in MCF-7 cells (MCF-7-T-bet).

208 ibited in Adriamycin (doxorubicin)-resistant MCF-7 cells (MCF-7/adr).

209 lar adhesion molecule (EpCAM) present on the MCF-7 cell membrane.

210 vidence demonstrating that CD24 expressed on MCF-7 cell membranes is responsible for rolling of the c

211 In MCF-7 cells Oct-1 binds the iNOS promoter, recruits RNA

212 However, the ligand that induces rolling of MCF-7 cells on E-selectin has not yet been identified, a

213 microarray profiling of the transcriptome of MCF-7 cells overexpressing miR-9 identified six novel di

214 of FOXM1 by RNAi abolished estrogen-induced MCF-7 cell proliferation and overcame acquired tamoxifen

215 regulations by ERalpha and a suppressor for MCF-7 cell proliferation.

216 Overexpression of MEK5 in MCF-7 cells promoted both hormone-dependent and hormone-

217 CXCR4 overexpression in MCF-7 cells promoted estrogen independence in vivo, wher

218 diated angiogenesis after exposure to ADP or MCF-7 cells providing a potential mechanism for how aspi

219 th of the OHT(R) cells, and its depletion in MCF-7 cells reduced sensitivity to tamoxifen in vitro an

220 nt acquisition of antiestrogen resistance by MCF-7 cells reflects selection of preexisting drug-resis

221 45-fold for MDA-MB-231 cells and 7-fold for MCF-7 cells, relative to untargeted PCCAs.

222 e evidence that HOXB7 overexpression renders MCF-7 cells resistant to tamoxifen via cross-talk betwee

223 n distal non-tumor tissue and low-metastatic MCF-7 cells, respectively.

224 c expression of constitutively active Akt in MCF-7 cells restored cell survival in S6K2-depleted cell

225 f plasma membrane and cytosolic nucleolin in MCF-7 cells resulted in a 3-fold decrease in AS1411 upta

226 se-3, but ectopic expression of caspase-3 in MCF-7 cells resulted in the cleavage of p70S6K.

227 Furthermore, the depletion of MLL1 in MCF-7 cells results in a dramatic decrease of chromatin

228 a- and glucocorticoid receptor (GR)-positive MCF-7 cells revealed that GR occupies several ERalpha-bi

229 Intravital imaging of CXCR4-expressing MCF-7 cells revealed that tumor cells migrate toward blo

230 The involvement of CD24 in MCF-7 cell rolling was confirmed by the rolling behavior

231 -IIB-GFP-, and 19% of NM-IIC1-GFP-expressing MCF-7 cells show multiple bleb formation, compared with

232 nockdown cell lines (derived from HCT116 and MCF-7 cells) showed increased apoptosis, G(2)/M arrest a

233 7 showing lower PLD2 activity, and MTLn3 and MCF-7 cells showing an elevated activity.

234 on affects breast cancer cells, we generated MCF-7 cells stably overexpressing StARD3-green fluoresce

235 ssibility, we generated K303R-overexpressing MCF-7 cells stably transfected with an aromatase express

236 OHT(R) cells and miR-221/222-overexpressing MCF-7 cells than in control cells, which suggests modula

237 Here, we investigate MCF-7 cells that are adapted to grow in acidic condition

238 rant IL-6 production and STAT3 activation in MCF-7 cells that constitutively express Twist, a metasta

239 MCF-7 cells that express Y14F are resistant to paclitaxe

240 latin failed to induce cleavage of p70S6K in MCF-7 cells that lack functional caspase-3, but ectopic

241 In this study, we selected MCF-7 cells that stably express forms of recombinant LOX

242 In MCF-7, cells that show the lowest level of PLD2 activity

243 nd for induction of CYP1B1 transcription (in MCF-7 cells), the recruitments of p300 and AhR, although

244 protein that overexpressed on the surface of MCF-7 cells, the aptamer conjugated MBs showed a predomi

245 In contrast, once taken up by MCF-7 cells, the iodide ligand is rapidly pumped out.

246 shown to be regulated by 17beta-estradiol in MCF-7 cells, the meta-analysis combined the statistical

247 ellular calcium also increased the growth of MCF-7 cells through an ER-dependent mechanism.

248 Here, we show that in breast cancer MCF-7 cells, TLE3, a co-repressor of the Groucho/Grg/TLE

249 Conversely, transfection of MCF-7 cells to express ROR1 reduced expression of E-cadh

250 Here we use MCF-7 cells to identify the organelles that Myo5c associ

251 tudies were conducted on human breast cancer MCF-7 cells to investigate both cellular uptake and cyto

252 on changed the architecture of breast cancer MCF-7 cells to that resembling MCF-10A cells, whereas ec

253 (Br)dU-carrying duplex DNA or (Br)dU-treated MCF-7 cells to UVB light could lead to the facile format

254 In MCF-7 cells transduced with Ad-GREB1 or transfected with

255 he effects of GREB1 on cell proliferation in MCF-7 cells transduced with Ad-GREB1 were also measured

256 mid, the activity was increased over 100% in MCF-7 cells transfected with a miR-328 antagomir, and di

257 Microarray analyses of MCF-7 cells transfected with control or SMRT small inter

258 Exposure of MCF-7 cells treated with 5 to 300 nm irradiation leads t

259 tivated cell sorting analysis suggested that MCF-7 cells treated with BME accumulated during the G2-M

260 interfering RNA-induced knockdown of p53 in MCF-7 cells treated with CPEC prevented cellular senesce

261 MCF-7 cells treated with EGF, ATP, extracellular calcium

262 ulted in an increase in turnover of FOXM1 in MCF-7 cells treated with the protein synthesis inhibitor

263 iple ceramide and dihydroceramide species in MCF-7 cells treated with TNFalpha occurred by up-regulat

264 sing small interfering RNA gene knockdown in MCF-7 cells triggered fibroblastic transformation and ce

265 NANOG induction promoted drug resistance in MCF-7 cells, tumor regeneration in Du145 cells and, most

266 found to reduce in vivo estrogen stimulated MCF-7 cell tumorigenesis using a xenograft mouse model.

267 bility maintenance of Rad51 requires TCTP in MCF-7 cells under normal cell culture conditions.

268 d by the decreased rolling velocities of the MCF-7 cells upon treatment with cytochalasin D (an inhib

269 level effects of 17beta-estradiol on single MCF-7 cells using Fourier transform infrared imaging spe

270 s of gene expression across time (2-96 h) in MCF-7 cell variants that were estrogen-dependent (WS8) o

271 Senescence in MCF-7 cells was associated with a G(2)- and S-phase arre

272 Using GRO-seq in MCF-7 cells, we defined the immediate transcriptional ef

273 CoCl2-induced EMT of human breast carcinoma MCF-7 cells, we found that TEPA, a copper chelator, inhi

274 f miR-21 in oncogenesis and chemoresistance, MCF-7 cells were also transfected with a specific anti-m

275 During the cell adhesion process, MCF-7 cells were consistently softer, exhibiting up to a

276 strict the study to genotypic effects, human MCF-7 cells were engineered to exclusively express allel

277 n of beta-catenin from the VE-cad complex by MCF-7 cells were lower than in MDA-MB-231 cells.

278 nts indicated that the effects of 3-OST3A in MCF-7 cells were mediated by altered interactions betwee

279 micropallet arrays in the presence of blood, MCF-7 cells were mixed into whole blood and added to sma

280 lates transcription of the ER gene promoter, MCF-7 cells were transiently transfected with a wild-typ

281 These processes were restored when MCF-7 cells were treated with beta(1)-activating antibod

282 To test this, MCF-7 cells were treated with doxorubicin or ionizing ra

283 When MCF-7 cells were treated with the analogues, those resul

284 TYR (named as MCF-7-TYR) and non-transfected MCF-7 cells were used as positive and negative controls,

285 ibroblasts (3T3-L1) and human breast cancer (MCF-7) cells were pre-treated with spice extracts and th

286 d cellular cytotoxicity of B16-F10, HeLa and MCF-7 cells when pre-incubated at lower pH, indicating T

287 e of HeLa cells expressing Cx43 or Cx46, and MCF-7 cells, which endogenously express Cx43 and Cx46.

288 lceramide levels declined after treatment of MCF-7 cells with a potent PKC activator, phorbol 12-myri

289 Of note, MCF-7 cells with acquired resistance to an IGF-1 recepto

290 th intrinsic tamoxifen resistance as well as MCF-7 cells with acquired tamoxifen and fulvestrant resi

291 Transfection of MCF-7 cells with antisense (AS) to miR-21 mimicked the E

292 ost cytotoxic compound reduced the growth of MCF-7 cells with IC(50) = 0.10 muM (cisplatin, 1.6 muM;

293 Treatment of MCF-7 cells with nicotine induced cell migration, wherea

294 We combined chromosomal interaction data in MCF-7 cells with our cohesin binding data to show that c

295 Transfection of MCF-7 cells with PKCepsilon or Nanog-specific small inte

296 In MCF-7 cells with stable RNAi-mediated suppression of JAR

297 1R activity in mitochondrial protection, and MCF-7 cells with suppressed IGF-1R activity became highl

298 Extended treatment of MCF-7 cells with tamoxifen resulted in progressively inc

299 Furthermore, co-treatment of MCF-7 cells with the PFKFB3 inhibitor and the anti-estro

300 lpha in tamoxifen- and fulvestrant-resistant MCF-7 cells, with pharmacologic inhibition of ERRalpha s